System and method for diagnosing and tracking congestive heart failure based on the periodicity of Cheyne-Stokes Respiration using an implantable medical device

ABSTRACT

Techniques are provided for distinguishing Cheyne-Stokes Respiration (CSR) caused by central sleep apnea (CSA) from CSR caused by congestive heart failure (CHF) and for evaluating the severity of CHF, if present, based up CSR. A time period associated with the CSR is determined based upon separate evaluation of apnea and hyperpnea periods during CSR and then the time period is compared against a time-varying discrimination threshold derived from integrated thoracic impedance signals. If the time period exceeds the threshold, the CSR of the patient is caused by CHF; otherwise, the CSR is caused by CSA. Thereafter, the course of therapy delivered to the patient is controlled based upon the type of CSR. In addition, if the CSR is caused by CHF, the time period associated with CSR is employed to determine the severity of CHF—with longer time periods being associated with more severe CHF.

CROSS-REFERENCE TO RELATED APPLICATIONS

This application is related to copending U.S. patent application Ser.No. 10/792,305, titled “System and Method for Diagnosing and TrackingCongestive Heart Failure Based on the Periodicity of Cheyne-StokesRespiration Using an Implantable Medical Device”, filed Mar. 2, 2004.

FIELD OF THE INVENTION

The invention generally relates to implantable medical devices, such aspacemakers or implantable cardioverter/defibrillators (ICDs) and, inparticular, to techniques for detecting congestive heart failure (CHF)and for evaluating its severity within a patient in which a medicaldevice is implanted.

BACKGROUND

CHF is a debilitating disease in which abnormal function of the heartleads to inadequate blood flow to fulfill the needs of the tissues andorgans of the body. Typically, the heart loses propulsive power becausethe cardiac muscle loses capacity to stretch and contract. Often, theventricles do not adequately fill with blood between heartbeats and thevalves regulating blood flow become leaky, allowing regurgitation orback-flow of blood. The impairment of arterial circulation deprivesvital organs of oxygen and nutrients. Fatigue, weakness and theinability to carry out daily tasks may result. Not all CHF patientssuffer debilitating symptoms immediately. Some may live actively foryears. Yet, with few exceptions, the disease is relentlesslyprogressive. As CHF progresses, it tends to become increasinglydifficult to manage. Even the compensatory responses it triggers in thebody may themselves eventually complicate the clinical prognosis. Forexample, when the heart attempts to compensate for reduced cardiacoutput, it adds muscle causing the ventricles to grow in volume in anattempt to pump more blood with each heartbeat. This places a stillhigher demand on the heart's oxygen supply. If the oxygen supply fallsshort of the growing demand, as it often does, further injury to theheart may result. The additional muscle mass may also stiffen the heartwalls to hamper rather than assist in providing cardiac output.

CHF has been classified by the New York Heart Association (NYHA) intofour classes of progressively worsening symptoms and diminished exercisecapacity. Class I corresponds to no limitation wherein ordinary physicalactivity does not cause undue fatigue, shortness of breath, orpalpitation. Class II corresponds to slight limitation of physicalactivity wherein such patients are comfortable at rest, but whereinordinary physical activity results in fatigue, shortness of breath,palpitations or angina. Class III corresponds to a marked limitation ofphysical activity wherein, although patients are comfortable at rest,even less than ordinary activity will lead to symptoms. Class IVcorresponds to inability to carry on any physical activity withoutdiscomfort, wherein symptoms of CHF are present even at rest and whereincreased discomfort is experienced with any physical activity.

In view of the potential severity of CHF, it is highly desirable todetect its onset as early as possible. One technique for identifying CHFis to detect Cheyne-Stokes Respiration (CSR), which is an abnormalrespiratory pattern often occurring in patients with CHF. CSR ischaracterized by alternating periods of apnea (i.e. a lack of breathing)and hyperpnea (i.e. fast, deep breathing.) Briefly, CSR arisesprincipally due to a time lag between blood carbon dioxide (CO₂) levelssensed by the respiratory control nerve centers of the brain and theblood CO₂ levels. With CHF, poor cardiac function results in poor bloodflow to the brain such that respiratory control nerve centers respond toblood CO₂ levels that are no longer properly representative of theoverall blood CO₂ levels in the body. Hence, the respiratory controlnerve centers trigger an increase in the depth and frequency ofbreathing in an attempt to compensate for perceived high blood CO₂levels whereas the blood CO₂ levels have already dropped. By the timethe respiratory control nerve centers detect the drop in blood CO₂levels and slow respiration in response, the blood CO₂ levels havealready increased. This cycle becomes increasingly unbalanced untilrespiration alternates between apnea and hyperpnea. The wildlyfluctuating blood chemistry levels can exacerbate CHF and other medicalconditions.

When CHF is still mild, CSR usually occurs, if at all, only while thepatient is sleeping. Hence, the detection of CSR during sleep can behelpful in detecting the onset of CHF. However, CSR during sleep canalso be caused by central sleep apnea (CSA), a neurogenic sleepdisorder. When blood CO₂ levels exceed a certain threshold, therespiratory control nerve center of the brain generates a burst of nervesignals for triggering inspiration. The nerve signals are relayed viaphrenic nerves to the diaphragm and via other nerves to chest wallmuscles, which collectively contract to expand the lungs. With CSA, thenerve signals are not properly generated for periods of time while thepatient is asleep or are of insufficient magnitude to trigger sufficientmuscle contraction to achieve inhalation. In either case, the patientthereby fails to inhale until appropriate respiratory nerve signals areeventually generated—at which point fast, deep breathing often occurs(i.e. hyperpnea) to compensate for the increased blood CO₂ levelsarising due to the episode of CSA. Often, the episodes of CSA are fairlyperiodic and so periods of apnea alternate with periods of hyperpnea. Inother words, CSR occurs.

Therapies can differ significantly depending upon whether the underlyingmedical condition causing CSR is CHF or is instead CSA. With CHF, drugtherapy is preferred, typically centered on medical treatment usingangiotensin converting enzyme (ACE) inhibitors, diuretics or digitalis.Cardiac resynchronization therapy (CRT) may also be employed, if abi-ventricular pacing device is implanted. Briefly, CRT seeks tonormalize asynchronous cardiac electrical activation and resultantasynchronous contractions associated with CHF by delivering synchronizedpacing stimulus to both ventricles, or to one ventricle upon detectionof intrinsic activity in the other ventricle. The stimulus issynchronized so as to help to improve overall cardiac function. This mayhave the additional beneficial effect of reducing the susceptibility tolife-threatening tachyarrhythmias. CRT and related therapies arediscussed in, for example, U.S. Pat. No. 6,643,546 to Mathis, et al.,entitled “Multi-Electrode Apparatus And Method For Treatment OfCongestive Heart Failure”; U.S. Pat. No. 6,628,988 to Kramer, et al.,entitled “Apparatus And Method For Reversal Of Myocardial RemodelingWith Electrical Stimulation”; and U.S. Pat. No. 6,512,952 to Stahmann,et al., entitled “Method And Apparatus For Maintaining SynchronizedPacing”. In contrast, to address CSA, an external breathing apparatus,such as a device providing continuous positive airway pressure (CPAP)therapy or bi-level positive pressure therapy (Bi-PAP), is employed.Overdrive pacing may be employed if a pacing device is implanted.Implantable phrenic nerve stimulators may be used as well to maintaininspiration during periods of CSA.

Accordingly, it would be desirable to provide techniques fordistinguishing between CHF-induced CSR and CSA-induced CSR, particularlyso that appropriate therapies can be exploited, and it is to this endthat certain aspects of the invention are directed. Herein, CSR inducedby CSA is also referred to as “CSR-CSA”; CSR induced by CHF is alsoreferred to as “CSR-CHF”.

An article entitled “The Entrainment of Low Frequency BreathingPeriodicity”, by Millar et al., (CHEST Vol. 98, No. 5, November 1990,pp. 1143–1148) provides data indicating that differences arise in theperiodicity of CSR depending up whether CSR-CSA or CSR-CHF. The datasuggests that the time period for CSR is higher in CSR-CHF patients thanin CSR-CSA patients (or that the frequency of CSR is lower). Althoughthe article does not suggest its exploitation within implantable medicalsystems, the periodicity of CSR, if properly detected, could potentiallybe used to distinguish CSR-CSA from CSR-CHF using an implantable medicaldevice and aspects of the invention are directed to that end.Challenges, moreover, remain in determining how best to detect andexploit CSR periodicity within an implantable system for distinguishingCSR-CSA from CSR-CHF. For example, arousal from sleep during CSR canaffect the measured periodicity of CSR, thus adversely affecting theviability of any discrimination technique based on CSR periodicity.Accordingly, other aspects of the invention are directed to specifictechniques for exploiting CSR periodicity for distinguishing CSR-CSAfrom CSR-CHF to provide reliable results for use in an implantablesystem.

Once it has been confirmed that CSR within a patient is induced by CHF,it is desirable to track the severity of CHF, particularly to facilitateselection of appropriate CHF therapies or to titrate such therapies. Thearticle by Millar et al. also provides data indicating that the timeperiod for CSR is correlated with circulation delay within patients(wherein circulation delay was defined as the average time delay forblood to travel from the lungs to a sensor in the carotid artery.) Sincea general increase in circulation delay within a patient is likely to beindicative of progression of CHF, the time period for CSR would appearto correlate with the severity of CHF. Although the article does notsuggest its exploitation within implantable medical systems, themagnitude of the periodicity of CSR, if properly detected, couldpotentially be used to track the severity of CHF using an implantablemedical device with patients subject to CSR-CHF. Hence, still otheraspects of the invention are directed to providing such capabilitywithin an implantable system. Again, however, challenges remain indetermining how best to detect and exploit the magnitude of the CSRperiodicity within an implantable system for tracking the severity ofCHF within patients subject to CSR-CHF. As mentioned above, arousal fromsleep or other movements occurring during CSR can affect the periodicityof CSR, thus adversely affecting the viability of any CHF trackingtechnique based on the magnitude of CSR periodicity. Accordingly, stillother aspects of the invention are directed to specific techniques forexploiting the magnitude of CSR periodicity for tracking CHF withinCSR-CHF patients so as provide reliable results for use in animplantable system.

It is worth noting that others have recognized that frequency and cyclelength of CSR may be used to measure the progression of CHF. See, U.S.Patent Application US2002/019367 of Cho et al. However, the patentapplication of Cho et al. does not appear to provide any indication ofhow frequency and cycle length are related to progression of CHF. Thereis no indication, for example, of whether an increase in CSR cyclelength indicates that CHF is progressing or whether it is a decrease inCSR cycle length that instead indicates that CHF is progressing. Inaddition, there does not appear to be any recognition that the CSRwithin a patient might be the result of CSA rather than CHF or thatarousal from sleep or other factors might significantly affect themanner by which frequency and cycle length are evaluated. Accordingly,it does not appear that the patent application to Cho et al. provides aviable system for tracking progression of CHF based on the periodicityof CSR, to which the present invention is directed.

SUMMARY

In accordance with a first embodiment, techniques are provided fordistinguishing CSR-CSA from CSR-CHF within a sleeping patient using animplanted medical device. Briefly, while the patient is asleep, aperiodicity associated with CSR is detected, and CSR-CSA isdistinguished from CSR-CHF based on an evaluation of the periodicity.Herein, CSR “periodicity” refers to either a time period of CSR or afrequency of CSR, which are reciprocal concepts.

In an exemplary embodiment, the time period for CSR is calculated bycombining an average duration of periods of sleep apnea during CSR withan average duration of bursts of breathing during CSR. The time periodis then compared with a CSR time period discrimination threshold. If thetime period exceeds the threshold, CSR-CHF is thereby detected;otherwise CSR-CSA is detected. Alternatively, a CSR frequency iscompared against a CSR frequency discrimination threshold. To preventcalculation of an erroneous value for the time period due to arousalfrom sleep, an accelerometer or other sensor is used to detect patientmovement and, if arousal is detected, the time period is rejected and anew time period is calculated once the patient resumes sleep and anotherepisode of CSR begins. The discrimination threshold is initiallycalculated based on thoracic impedance. More specifically, signalsrepresentative of thoracic impedance sensed using leads implanted withinthe heart are low-pass filtered. The derivative of the filteredimpedance signal is calculated and then zero-crossing points areidentified. The derivative of the filtered impedance signal is thenintegrated between each pair of consecutive zero-crossing points togenerate a set of integral values, which effectively restorevalley-top-peak amplitudes. A moving average of the integrated values isthen periodically updated for use as the discrimination threshold.

Therapy is then delivered depending up whether the CSR is caused by CSAor instead by CHF. If CSR is caused by CSA, overdrive pacing may beemployed in an attempt to prevent further episodes of CSA for occurringto thereby prevent further episodes of CSR from occurring. Alternately,if an implantable drug pump is provided, appropriate anti-apneamedications may be delivered to the patient. If overdrive pacing or drugtherapy fails to prevent the onset of additional episodes of CSA, animplantable alarm or an external bedside alarm is preferably employed togenerate a warning signal to the patient to awaken the patient so as toterminate the episode of apnea and thereby prevent the onset of CSR-CSA.Alternatively, if a phrenic nerve stimulator is provided, rhythmicstimulation may be applied to the phrenic nerves to stimulate thediaphragm so as to mimic respiration, thus overcoming apnea andpreventing the onset of CSR.

If CSR is instead caused by CHF, then CRT is preferably employed toimprove cardiac function. Additionally, or in the alternative, overdrivepacing or drug therapy may be provided. As with CSR-CSA, if additionalepisodes of CSR develop, warning alarms are preferably employed toawaken the patient during periods CSR to awaken the patient to break thecycle of CSR and help stabilize blood chemistry levels.

In accordance with a second embodiment, techniques are provided forevaluating the severity of CHF within a patient suffering from CSR-CHF,again using an implanted medical device. Briefly, a periodicityassociated with CSR is detected. The severity of CHF within the patientis evaluated based on the periodicity, with a relatively long CSR timeperiod being indicative of more severe CHF than a relatively short CSRtime period (or with a relatively low CSR frequency being indicative ofmore severe CSR than a relatively high frequency.)

In an exemplary embodiment, the periodicity for CSR is compared againsta set of values representative of various levels of CHF, then CHFtherapy is controlled based on the degree of severity. For example,control parameters for CRT may be adjusted based on the severity of CHF.Additionally, or in the alternative, the aggressiveness of overdrivepacing may be controlled or drug dosages provided via an implantabledrug pump may be titrated based on the severity of CHF. As with thetechniques summarized above, if additional episodes of CSR neverthelessdevelop, warning alarms are preferably employed to alert the patientduring periods CSR to break the cycle of CSR and thereby help stabilizeblood chemistry levels. In addition, techniques are provided forassessing the severity of CSR by using a trend derived from CSRperiodicity (either duration or occurrences).

Thus, various techniques are provided for use with implantable medicaldevice for discriminating CSR-CSA from CSR-CHF within a patient and forevaluating the severity of CHF within the patient, if subject toCSR-CHF. Other objects, features and advantages of the invention will beapparent from the detailed description to follow.

BRIEF DESCRIPTION OF THE DRAWINGS

The above and further features, advantages and benefits of the presentinvention will be apparent upon consideration of the present descriptiontaken in conjunction with the accompanying drawings, in which:

FIG. 1 illustrates pertinent components of an implantable CSR responsivemedical system having a pacemaker or ICD capable of detecting episodesof CSR, distinguishing CSR-CSA from CSR-CHF based on CSR periodicity anddelivering therapy in response thereto and also capable of tracking theseverity of CHF also based on CSR periodicity;

FIG. 2 is a flow diagram providing an overview of the method fordiscriminating between CSR-CHF and CSR-CSA as performed by the system ofFIG. 1;

FIG. 3 is a stylized diagram of episodes of CSR illustrating thedifferences in the CSR periodicity between CSR-CHF and CSR-CSA;

FIG. 4 is a flow diagram providing an overview of the method fortracking severity of CHF based on CSR periodicity as performed by thesystem of FIG. 1;

FIG. 5 is a stylized diagram of episodes of CSR illustrating theincrease in CHF severity associated with an increase in CSR time periodfor CSR-CHF;

FIG. 6 is a simplified, partly cutaway view, illustrating the pacer/ICDof FIG. 1 along with at set of leads implanted into the heart of thepatient;

FIG. 7 is a functional block diagram of the pacer/ICD of FIG. 6,illustrating basic circuit elements that provide cardioversion,defibrillation and/or pacing stimulation in four chambers of the heartand particularly illustrating components for distinguishing CSR-CSA fromCSR-CHF and for controlling delivery of therapy in response thereto andfor tracking the severity of CHF;

FIG. 8 is a functional block diagram of selected components of thepacemaker or ICD of FIG. 7, particularly illustrating a CSRperiodicity-based CSR discrimination unit, a CSA/CHF therapy controllerand a CSR periodicity-based CHF evaluation unit;

FIG. 9 is a flow diagram illustrating an exemplary method performed bythe implanted device of FIG. 7 for distinguishing CSR-CSA from CSR-CHFbased on a CSR time period derived from monitoring thoracic impedance;

FIG. 10 is a stylized diagram of an episode of CSR illustratingimpedance (Z), impedance differential (dZ) and integrated dZ;

FIG. 11 is a flow diagram illustrating an exemplary method performed bythe implanted device of FIG. 7 for determining a CSR time perioddiscrimination threshold for use in the method of FIG. 9;

FIG. 12 is a flow diagram illustrating an exemplary method performed bythe implanted system of FIG. 7 for delivering therapy in response to adetermination that CSR is induced by CSA;

FIG. 13 is a flow diagram illustrating an exemplary method performed bythe implanted system of FIG. 7 for delivering therapy in response to adetermination that CSR is induced by CHF; and

FIG. 14 is a flow diagram illustrating an exemplary method performed bythe implanted device of FIG. 7 for evaluating the severity of CHF basedon CSR periodicity derived from monitoring thoracic impedance.

DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS

The following description includes the best mode presently contemplatedfor practicing the invention. This description is not to be taken in alimiting sense but is made merely to describe general principles of theinvention. The scope of the invention should be ascertained withreference to the issued claims. In the description of the invention thatfollows, like numerals or reference designators will be used to refer tolike parts or elements throughout.

Overview of Implantable CSR Responsive System

FIG. 1 illustrates an implantable CSR responsive medical system 8capable of detecting individual episodes of CSR, discriminating betweenCSR-CSA and CSR-CHF, evaluating the severity of CHF and deliveringappropriate therapy. CSR responsive system 8 includes a pacer/ICD 10 orother cardiac stimulation device that incorporates internal components(shown individually in FIGS. 7 and 8) to that end. More specifically,pacer/ICD 10 receives signals from various cardiac pacing leads fromwhich thoracic impedance is derived. In FIG. 1, only one exemplary lead12 is shown. Others pacing leads are shown in FIG. 6. Based onvariations in thoracic impedance based by respiration, the pacer/ICDdetects individual episodes of CSR, calculates the periodicityassociated with the episodes of CSR and determines whether theindividual episodes of CSR are caused by CSA or CHF based on theperiodicity, so that appropriate therapy can be provided. For episodesof CSR caused by CHF, the pacer/ICD also evaluates the severity of CHFbased on the periodicity. The pacer/ICD also tracks the progression ofCHF based on any changes over time occurring in the CSR periodicityevaluated during CSR-CHF. Detailed descriptions of these techniques areset forth below.

If episodes of CSR are found to be caused by CHF, then appropriatetherapy is automatically delivered by pacer/ICD. For example, CRTtherapy may be applied using leads implanted in the ventricles so as toimprove cardiac function in an effort to prevent additional episodes ofCSR-CHF from occurring as well as to gain the other benefits of CRT.Additionally, or in the alternative, the implantable CSR responsivesystem may be equipped with a drug pump 14 capable of the deliveringdrug therapy in an attempt to address the underlying CHF. Discussions ofpossible medications for use in CHF patients are provided below. Inaddition, the pacer/ICD may be used to deliver DAO pacing for thepurposes of preventing additional episodes of CSR-CHF from occurring.Control parameters for DAO and CRT therapy are adjusted based on theseverity of the underlying CHF. Any drug dosages provided by animplantable drug pump may be titrated based on the severity of CHF.Hence, upon the detection of initial episodes of CSR-CHF, DAO and/ordrug therapy is preferably delivered to the patient in an attempt toprevent the onset of additional episodes of CSR. If additional episodesnevertheless occur, then warning signals are generated using an eitherinternal CSR alarm 16 or an external bedside alarm 18 to awaken thepatient during CSR in an attempt to restore normal breathing and tothereby equalize blood chemistry levels. Internal alarm 16 may be avibrating device or a “tickle” voltage device that, in either case,provides perceptible stimulation to the patient to awaken the patient.The bedside alarm may provide audible or visual alarm signals ofsufficient magnitude to awaken the patient. In additional, once CSR-CHFhas been detected, diagnostic in formation is stored for subsequentreview by a physician or other medial professional. The physician maythen prescribe any other appropriate therapies to address the CSR andthe underlying CHF. The physician may also adjust the operation of thepacer/ICD to activate, deactivate or otherwise control any therapiesthat are automatically applied.

If the episodes of CSR are instead found to be caused by CSA, then CSAtherapy is automatically delivered by pacer/ICD. If equipped with a drugpump, drug therapy may be delivered in an attempt to prevent additionalepisodes CSA to thereby prevent CSR-CSA. Discussions of possiblemedications for use with CSA are provided below. The pacer/ICD may alsobe deliver DAO pacing for the purposes of preventing additional episodesof CSA from occurring. As with CSR-CHF therapy, control parameters forDAO and CRT therapy applied to address CSR-CSA may be controlled basedon the severity of the CSR. In addition, any drug dosages provided by animplantable drug pump to address CSA may be titrated based on theperiodicity of the resulting CSR. Again, DAO and/or drug therapy ispreferably delivered to the patient first in an attempt to prevent theonset of additional episodes of CSR. If additional episodes neverthelessoccur, then warning signals are generated using either the internal CSRalarm or the external bedside alarm to awaken the patient during CSR-CSAto restore normal breathing and thereby equalize blood chemistry levels.

Although not shown, if the patient suffers from chronic CSA, implantablephrenic nerve stimulators may be implanted for use in responding toindividual episodes of CSA. When an episode of CSA is detected, thepacer/ICD controls the phrenic nerve stimulators to rhythmicallystimulate the diaphragm to cause the diaphragm to contract, thusmimicking breathing and thereby preventing CSR from arising as a resultof CSA. The use of phrenic nerve stimulators are preferable withinpatients suffering from chronic CSA to allow individual episodes of CSAto be terminated before CSA causes CSR to occur so as to avoid the needto repeatedly awaken the patient. Techniques for detecting and treatingsleep apnea are set forth in U.S. Patent Application: 2003/0153954 A1 ofPark et al., entitled “Sleep Apnea Therapy Device Using DynamicOverdrive Pacing”.

Hence, FIG. 1 provides an overview of an implantable system fordetecting individual episodes of CSR, discriminating between CSR-CSA andCSR-CHF, evaluating the severity of CHF if it is the cause of CSR, anddelivering appropriate therapy. Internal signal transmission linesprovided for interconnecting the various implanted components are notshown. Wireless signal transmission may alternatively be employed. Inaddition, it should be appreciated that systems provided in accordancewith invention need not include all the components shown in FIG. 1. Inmany cases, for example, the system will include only the pacer/ICD andits leads with all therapy provide in the form of DAO or CRT. Drug pumpsand CSR alarms are not necessarily implanted. Other implementations mayemploy phrenic nerve stimulators, but no internal or external alarms andno drug pumps. These are just a few exemplary embodiments. No attempt ismade herein to describe all possible combinations of components that maybe provided in accordance with the general principles of the invention.In addition, the particular locations of the implanted components shownin FIG. 1 are merely illustrative and may not correspond to actualimplant location.

Overview of CSR Discrimination Technique

FIG. 2 provides an overview of the CSR discrimination technique of theinvention. Initially, at step 100, the implantable pacer/ICD detects anepisode of CSR while the patient is asleep then determines theperiodicity associated with CSR. The technique is performed while thepatient is asleep because CSR-CSA only occurs while a patient is asleep(since it arises due to a neurogenic disorder that only occurs duringsleep.) In other words, if CSR occurs while a patient is awake, itshould be due to CHF and so discrimination between CSR-CSA and CSR-CHFshould not be required. The only time such discrimination is typicallyrequired is if CSR occurs while the patient is asleep. Note that CSR-CHFis far more common than CSR-CSA. Nevertheless, since the therapies to beapplied may differ, it is desirable to discriminate between the twobefore delivering therapy.

FIG. 3 illustrates exemplary time periods for both CSR-CSA respirationand CSR-CHF respiration. As can be seen, CSR is characterized byintermittent bursts of heavy, deep breathing or hyperpnea 104 separatedby periods of sleep apnea 106. Generally speaking, the time period ofCSR is the duration from the onset of one breathing cluster to the onsetof a next breathing cluster. This time period is also equal to the sumof an apnea time period and the subsequent respiration burst timeperiod. As illustrated, a time period 108 of CSR-CHF is significantlylonger than a time period 110 for CSR-CSA. Accordingly, the CSRperiodicity provides a basis for discriminating CSR-CSA from CSR-CHF. Adiscrimination time period threshold duration 112, calculated inaccordance with techniques described below, provides a basis fordiscriminating CSR-CSA from CSR-CHF. If the time period for a particularepisode of CSR exceeds the threshold, then the pacer/ICD concludes thatit is likely that the episode of CSR was caused by an underlying CHF.Otherwise, it is likely that the episode of CSR is caused by periods ofCSA, possibly unrelated to CHF. Alternatively, CSR frequency can insteadbe evaluated and compared against a CSR frequency discriminationthreshold. Also, note that the CSR respiration patterns shown in FIG. 3are stylized so as to more clearly illustrate pertinent features therespiration patterns and should not be construed as representing actualclinically-detected CSR respiration patterns.

Returning to FIG. 2, the pacer/ICD compares the CSR periodicity, at step112, for the episode of CSR against the appropriate discriminationthreshold to identify the source of the episode of CSR. Then, at step114, appropriate therapy is delivered and diagnostic data is recorded.As already explained, various types of therapy may be delivered, aloneor in combination, depending upon the capabilities of the implantedsystem. Note that, for most patients, episodes of CSR either are all theresult of an underlying CHF or are all the result of periodic episodesof CSA. Hence, once a determination has been made as to whether thepatient is suffering from CSR-CSA or CSR-CHF, this determination neednot be repeated, at least in the short-term. Accordingly, from manypatients, once the source of CSR has been identified, it is sufficientto evaluate additional episodes of CSR only infrequently (e.g. every fewweeks or months) to determine a change in status of the patient. In oneexample, the pacer/ICD analyzes all episodes of CSR for several weeksand, if all are caused by the same underlying source, the pacer/ICDswitches its mode of operation to only analyze CSR episodes every fewweeks to verify that the episodes are still all caused by the sameunderlying source. If the patient ultimately begins to develop mixedepisodes of CSR, then the pacer/ICD switches its mode of operation toagain analyze each individual episode of CSR to identify its particularcause so that appropriate diagnostic information may be stored andappropriate therapy may be delivered. A determination can be made, forexample, whether a majority of the episodes of CSR are caused by CSA orcaused by CHF and therapy adjusted accordingly. Specific strategies fordelivering therapy are set forth below.

Thus, FIGS. 2–3 provide an overview of the CSR discrimination techniqueof the invention. In the following, an overview of the CHF severityevaluation technique is provided.

Overview of CHF Severity Evaluation Technique

FIG. 4 provides an overview of the CHF severity evaluation technique ofthe invention. The technique may be performed in addition to the CSRdiscrimination technique of FIG. 2 or may be implemented independently.Beginning at step 150, the pacer/ICD detects a periodicity associatedwith the CSR for the patient. The patient need not be asleep. Shouldepisodes of CSR occur while the patient is awake, as commonly happens inpatients with fairly severe CHF, the severity of CHF may be evaluatedbased upon such episodes. If CSR only occurs while the patient isasleep, then the evaluation of the severity of CHF is made based uponCSR episodes occurring while asleep.

FIG. 5 illustrates CSR time periods for CSR-CHF respiration patterns forvarious levels of CHF severity ranging from mild to severe. Again, eachCSR respiratory pattern includes alternating periods of apnea 152followed by brief bursts of hyperpnea 154. As can be seen, CSR timeperiods are comparatively shorter for patients with mild CHF andconsiderably longer for patients with more severe CHF. This occursbecause circulation delays caused by poor cardiac function due to CHFresult in longer feedback loops between the time when the respiratorycontrol centers of the brain sense changes in blood chemistry and thetime when those changes in blood chemistry actually occur in the lungs.The longer periods of apnea occurring within patients with severe CHFresult in far more significant variations in blood chemistry levels,which tend to exacerbate CHF as well as other medical conditions. In anycase, by determining the periodicity for CSR, the severity of CHF canthereby be evaluated. Note that the CSR respiration patterns shown inFIG. 5 are stylized so as to more clearly illustrate pertinent featuresthe respiration patterns and should not be construed as representingactual clinically-detected CSR respiration patterns.

Returning to FIG. 4, the evaluation of CHF severity is performed at step156 based upon the CSR periodicity detected at step 150—with long CSRtime periods being indicative of severe CHF and relatively short timeperiods being indicative of mild CHF (or with low CSR frequency beingindicative of sever CHF and relatively high CSR frequency beingindicative of mild CHF.) As explained below, a look-up table of rangesof periodicity values may be accessed, which correspond to the variouslevels of CHF severity. In any case, once the severity of CHF has beenevaluated then, at step 158, CHF therapy is delivered based upon theseverity of CHF and appropriate diagnostic data is recorded. Valuesindicative of the severity of CHF are preferably stored within thepacer/ICD so that the progression of CHF may be tracked, at step 159,over an extended period of time, within increasing values for the CSRtime period indicative of progression of CHF. As the disease progresses,the pacer/ICD automatically adjusts CHF therapy by, for example,adjusting CRT control parameters or titrating dosages of any medicationsautomatically delivered via the implanted drug pump. Typically, theseverity of CHF does not change significantly over a few days or weeksand hence it is usually sufficient for the pacer/ICD to evaluate theseverity of CHF at most only once every few weeks. To ensure that anyshort term changes in patient status to not improperly affect thetracking of CHF progression, periodicity values for CSR-CHF are averagedover a relatively large number of CSR episodes occurring under similarconditions. In one example, only episodes of CSR occurring while thepatient is asleep are employed for use in generating an averageperiodicity value for CHF severity evaluation. In another example, onlyepisodes of CSR occurring while the patient is awake are employed.

Thus, the FIGS. 4–5 provide an overview of the CSR-CHF severityevaluation techniques of the invention. In the following section, anexemplary pacer/ICD will be described, which includes components forperforming the CSR discrimination technique of FIGS. 2–3 as well as theCHF severity evaluation technique of FIGS. 4–5.

Pacer/ICD

With reference to FIGS. 6 and 7, a detailed description of the pacer/ICDof FIG. 1 will now be provided. FIG. 6 provides a simplified blockdiagram of the pacer/ICD, which is a dual-chamber stimulation devicecapable of treating both fast and slow arrhythmias with stimulationtherapy, including cardioversion, defibrillation, and pacingstimulation, as well as capable of detecting CSR, discriminating CSR-CSAfrom CSR-CHF, evaluating the severity of CHF based on CSR-CHF, andcontrolling delivering of therapy in response thereto.

To provide atrial chamber pacing stimulation and sensing, pacer/ICD 10is shown in electrical communication with a heart 212 by way of a leftatrial lead 220 having an atrial tip electrode 222 and an atrial ringelectrode 223 implanted in the atrial appendage. Pacer/ICD 10 is also inelectrical communication with the heart by way of a right ventricularlead 230 having, in this embodiment, a ventricular tip electrode 232, aright ventricular ring electrode 234, a right ventricular (RV) coilelectrode 236, and a superior vena cava (SVC) coil electrode 238.Typically, the right ventricular lead 230 is transvenously inserted intothe heart so as to place the RV coil electrode 236 in the rightventricular apex, and the SVC coil electrode 238 in the superior venacava. Accordingly, the right ventricular lead is capable of receivingcardiac signals, and delivering stimulation in the form of pacing andshock therapy to the right ventricle.

To sense left atrial and ventricular cardiac signals and to provide leftchamber pacing therapy, pacer/ICD 10 is coupled to a “coronary sinus”lead 224 designed for placement in the “coronary sinus region” via thecoronary sinus os for positioning a distal electrode adjacent to theleft ventricle and/or additional electrode(s) adjacent to the leftatrium. As used herein, the phrase “coronary sinus region” refers to thevasculature of the left ventricle, including any portion of the coronarysinus, great cardiac vein, left marginal vein, left posteriorventricular vein, middle cardiac vein, and/or small cardiac vein or anyother cardiac vein accessible by the coronary sinus. Accordingly, anexemplary coronary sinus lead 224 is designed to receive atrial andventricular cardiac signals and to deliver left ventricular pacingtherapy using at least a left ventricular tip electrode 226, left atrialpacing therapy using at least a left atrial ring electrode 227, andshocking therapy using at least a left atrial coil electrode 228. Withthis configuration, biventricular pacing can be performed. Although onlythree leads are shown in FIG. 6, it should also be understood thatadditional stimulation leads (with one or more pacing, sensing and/orshocking electrodes) may be used in order to efficiently and effectivelyprovide pacing stimulation to the left side of the heart or atrialcardioversion and/or defibrillation.

A simplified block diagram of internal components of pacer/ICD 10 isshown in FIG. 7. While a particular pacer/ICD is shown, this is forillustration purposes only, and one of skill in the art could readilyduplicate, eliminate or disable the appropriate circuitry in any desiredcombination to provide a device capable of treating the appropriatechamber(s) with cardioversion, defibrillation and pacing stimulation aswell as providing for the aforementioned apnea detection and therapy.

The housing 240 for pacer/ICD 10, shown schematically in FIG. 7, isoften referred to as the “can”, “case” or “case electrode” and may beprogrammably selected to act as the return electrode for all “unipolar”modes. The housing 240 may further be used as a return electrode aloneor in combination with one or more of the coil electrodes, 228, 236 and238, for shocking purposes. The housing 240 further includes a connector(not shown) having a plurality of terminals, 242, 243, 244, 246, 248,252, 254, 256 and 258 (shown schematically and, for convenience, thenames of the electrodes to which they are connected are shown next tothe terminals). As such, to achieve right atrial sensing and pacing, theconnector includes at least a right atrial tip terminal (A_(R) TIP) 242adapted for connection to the atrial tip electrode 222 and a rightatrial ring (A_(R) RING) electrode 243 adapted for connection to rightatrial ring electrode 223. To achieve left chamber sensing, pacing andshocking, the connector includes at least a left ventricular tipterminal (V_(L) TIP) 244, a left atrial ring terminal (A_(L) RING) 246,and a left atrial shocking terminal (A_(L) COIL) 248, which are adaptedfor connection to the left ventricular ring electrode 226, the leftatrial tip electrode 227, and the left atrial coil electrode 228,respectively. To support right chamber sensing, pacing and shocking, theconnector further includes a right ventricular tip terminal (V_(R) TIP)252, a right ventricular ring terminal (V_(R) RING) 254, a rightventricular shocking terminal (R_(V) COIL) 256, and an SVC shockingterminal (SVC COIL) 258, which are adapted for connection to the rightventricular tip electrode 232, right ventricular ring electrode 234, theRV coil electrode 236, and the SVC coil electrode 238, respectively.

At the core of pacer/ICD 10 is a programmable microcontroller 260, whichcontrols the various modes of stimulation therapy. As is well known inthe art, the microcontroller 260 (also referred to herein as a controlunit) typically includes a microprocessor, or equivalent controlcircuitry, designed specifically for controlling the delivery ofstimulation therapy and may further include RAM or ROM memory, logic andtiming circuitry, state machine circuitry, and I/O circuitry. Typically,the microcontroller 260 includes the ability to process or monitor inputsignals (data) as controlled by a program code stored in a designatedblock of memory. The details of the design and operation of themicrocontroller 260 are not critical to the invention. Rather, anysuitable microcontroller 260 may be used that carries out the functionsdescribed herein. The use of microprocessor-based control circuits forperforming timing and data analysis functions are well known in the art.

As shown in FIG. 7, an atrial pulse generator 270 and a ventricularpulse generator 272 generate pacing stimulation pulses for delivery bythe right atrial lead 220, the right ventricular lead 230, and/or thecoronary sinus lead 224 via an electrode configuration switch 274. It isunderstood that in order to provide stimulation therapy in each of thefour chambers of the heart, the atrial and ventricular pulse generators,270 and 272, may include dedicated, independent pulse generators,multiplexed pulse generators or shared pulse generators. The pulsegenerators, 270 and 272, are controlled by the microcontroller 260 viaappropriate control signals, 276 and 278, respectively, to trigger orinhibit the stimulation pulses.

The microcontroller 260 further includes timing control circuitry (notseparately shown) used to control the timing of such stimulation pulses(e.g., pacing rate, atrio-ventricular (AV) delay, atrial interconduction(A—A) delay, or ventricular interconduction (V—V) delay, etc.) as wellas to keep track of the timing of refractory periods, blankingintervals, noise detection windows, evoked response windows, alertintervals, marker channel timing, etc., which is well known in the art.Switch 274 includes a plurality of switches for connecting the desiredelectrodes to the appropriate I/O circuits, thereby providing completeelectrode programmability. Accordingly, the switch 274, in response to acontrol signal 280 from the microcontroller 260, determines the polarityof the stimulation pulses (e.g., unipolar, bipolar, combipolar, etc.) byselectively closing the appropriate combination of switches (not shown)as is known in the art. Moreover, as the explained in greater detailbelow, the microcontroller transmits signals to controlling the switchto connect a different set of electrodes during a far-field overdrivepacing than during near-field overdrive pacing.

Atrial sensing circuits 282 and ventricular sensing circuits 284 mayalso be selectively coupled to the right atrial lead 220, coronary sinuslead 224, and the right ventricular lead 230, through the switch 274 fordetecting the presence of cardiac activity in each of the four chambersof the heart. Accordingly, the atrial (ATR. SENSE) and ventricular (VTR.SENSE) sensing circuits, 282 and 284, may include dedicated senseamplifiers, multiplexed amplifiers or shared amplifiers. The switch 274determines the “sensing polarity” of the cardiac signal by selectivelyclosing the appropriate switches, as is also known in the art. In thisway, the clinician may program the sensing polarity independent of thestimulation polarity. Each sensing circuit, 282 and 284, preferablyemploys one or more low power, precision amplifiers with programmablegain and/or automatic gain control, bandpass filtering, and a thresholddetection circuit, as known in the art, to selectively sense the cardiacsignal of interest. The automatic gain control enables pacer/ICD 10 todeal effectively with the difficult problem of sensing the low amplitudesignal characteristics of atrial or ventricular fibrillation. Theoutputs of the atrial and ventricular sensing circuits, 282 and 284, areconnected to the microcontroller 260 which, in turn, are able to triggeror inhibit the atrial and ventricular pulse generators, 270 and 272,respectively, in a demand fashion in response to the absence or presenceof cardiac activity in the appropriate chambers of the heart.

For arrhythmia detection, pacer/ICD 10 utilizes the atrial andventricular sensing circuits, 282 and 284, to sense cardiac signals todetermine whether a rhythm is physiologic or pathologic. As used herein“sensing” is reserved for the noting of an electrical signal, and“detection” is the processing of these sensed signals and noting thepresence of an arrhythmia. The timing intervals between sensed events(e.g., P-waves, R-waves, and depolarization signals associated withfibrillation which are sometimes referred to as “F-waves” or“Fib-waves”) are then classified by the microcontroller 260 by comparingthem to a predefined rate zone limit (i.e., bradycardia, normal, atrialtachycardia, atrial fibrillation, low rate VT, high rate VT, andfibrillation rate zones) and various other characteristics (e.g., suddenonset, stability, physiologic sensors, and morphology, etc.) in order todetermine the type of remedial therapy that is needed (e.g., bradycardiapacing, antitachycardia pacing, cardioversion shocks or defibrillationshocks).

Cardiac signals are also applied to the inputs of an analog-to-digital(A/D) data acquisition system 290. The data acquisition system 290 isconfigured to acquire intracardiac electrogram signals, convert the rawanalog data into a digital signal, and store the digital signals forlater processing and/or telemetric transmission to an external device302. The data acquisition system 290 is coupled to the right atrial lead220, the coronary sinus lead 224, and the right ventricular lead 230through the switch 274 to sample cardiac signals across any pair ofdesired electrodes. The microcontroller 260 is further coupled to amemory 294 by a suitable data/address bus 296, wherein the programmableoperating parameters used by the microcontroller 260 are stored andmodified, as required, in order to customize the operation of pacer/ICD10 to suit the needs of a particular patient. Such operating parametersdefine, for example, pacing pulse amplitude or magnitude, pulseduration, electrode polarity, rate, sensitivity, automatic features,arrhythmia detection criteria, and the amplitude, waveshape and vectorof each shocking pulse to be delivered to the patient's heart withineach respective tier of therapy. Other pacing parameters include baserate, rest rate and circadian base rate.

Advantageously, the operating parameters of the implantable pacer/ICD 10may be non-invasively programmed into the memory 294 through a telemetrycircuit 300 in telemetric communication with the external device 302,such as a programmer, transtelephonic transceiver or a diagnostic systemanalyzer. The telemetry circuit 300 is activated by the microcontrollerby a control signal 306. The telemetry circuit 300 advantageously allowsintracardiac electrograms and status information relating to theoperation of pacer/ICD 10 (as contained in the microcontroller 260 ormemory 294) to be sent to the external device 302 through an establishedcommunication link 304. Pacer/ICD 10 further includes an accelerometeror other physiologic sensor 308, commonly referred to as a“rate-responsive” sensor because it is typically used to adjust pacingstimulation rate according to the exercise state of the patient.However, the physiological sensor 308 may further be used to detectchanges in cardiac output, changes in the physiological condition of theheart, or diurnal changes in activity (e.g., detecting sleep and wakestates) and to detect arousal from sleep. Accordingly, themicrocontroller 260 responds by adjusting the various pacing parameters(such as rate, AV Delay, V—V Delay, etc.) at which the atrial andventricular pulse generators, 270 and 272, generate stimulation pulses.While shown as being included within pacer/ICD 10, it is to beunderstood that the physiologic sensor 308 may also be external topacer/ICD 10, yet still be implanted within or carried by the patient. Acommon type of rate responsive sensor is an activity sensorincorporating an accelerometer or a piezoelectric crystal, which ismounted within the housing 240 of pacer/ICD 10. Other types ofphysiologic sensors are also known, for example, sensors that sense theoxygen content of blood, respiration rate and/or minute ventilation, pHof blood, ventricular gradient, etc. However, any sensor may be usedwhich is capable of sensing a physiological parameter that correspondsto the exercise state of the patient an, in particular, is capable ofdetecting arousal from sleep or other movement.

The pacer/ICD additionally includes a battery 310, which providesoperating power to all of the circuits shown in FIG. 7. The battery 310may vary depending on the capabilities of pacer/ICD 10. If the systemonly provides low voltage therapy, a lithium iodine or lithium copperfluoride cell may be utilized. For pacer/ICD 10, which employs shockingtherapy, the battery 310 must be capable of operating at low currentdrains for long periods, and then be capable of providing high-currentpulses (for capacitor charging) when the patient requires a shock pulse.The battery 310 must also have a predictable discharge characteristic sothat elective replacement time can be detected. Accordingly, pacer/ICD10 is preferably capable of high voltage therapy and appropriatebatteries.

As further shown in FIG. 7, pacer/ICD 10 is shown as having an impedancemeasuring circuit 312 which is enabled by the microcontroller 260 via acontrol signal 314. Herein, thoracic impedance is primarily detected foruse in tracking thoracic respiratory oscillations. Other uses for animpedance measuring circuit include, but are not limited to, leadimpedance surveillance during the acute and chronic phases for properlead positioning or dislodgement; detecting operable electrodes andautomatically switching to an operable pair if dislodgement occurs;measuring respiration or minute ventilation; measuring thoracicimpedance for determining shock thresholds; detecting when the devicehas been implanted; measuring stroke volume; and detecting the openingof heart valves, etc. The impedance measuring circuit 120 isadvantageously coupled to the switch 74 so that any desired electrodemay be used.

In the case where pacer/ICD 10 is intended to operate as an implantablecardioverter/defibrillator (ICD) device, it detects the occurrence of anarrhythmia, and automatically applies an appropriate electrical shocktherapy to the heart aimed at terminating the detected arrhythmia. Tothis end, the microcontroller 260 further controls a shocking circuit316 by way of a control signal 318. The shocking circuit 316 generatesshocking pulses of low (up to 0.5 joules), moderate (0.5–10 joules) orhigh energy (11 to 40 joules), as controlled by the microcontroller 260.Such shocking pulses are applied to the heart of the patient through atleast two shocking electrodes, and as shown in this embodiment, selectedfrom the left atrial coil electrode 228, the RV coil electrode 236,and/or the SVC coil electrode 238. The housing 240 may act as an activeelectrode in combination with the RV electrode 236, or as part of asplit electrical vector using the SVC coil electrode 238 or the leftatrial coil electrode 228 (i.e., using the RV electrode as a commonelectrode). Cardioversion shocks are generally considered to be of lowto moderate energy level (so as to minimize pain felt by the patient),and/or synchronized with an R-wave and/or pertaining to the treatment oftachycardia. Defibrillation shocks are generally of moderate to highenergy level (i.e., corresponding to thresholds in the range of 5–40joules), delivered asynchronously (since R-waves may be toodisorganized), and pertaining exclusively to the treatment offibrillation. Accordingly, the microcontroller 260 is capable ofcontrolling the synchronous or asynchronous delivery of the shockingpulses.

Microcontroller 260 also includes various components directed to thedetection and treatment of CSR-CSA or CSR-CHF. More specifically, themicrocontroller includes a CSR periodicity-based discrimination unit 301for distinguishing CSR-CSA from CSR-CHF. A CSA/CHF therapy controller303 delivers appropriate therapy in response to the determination. Ifthe CSR is caused by CHF, a CSR periodicity-based CHF evaluation unit305 operates to evaluate the severity of CHF, so that appropriatediagnostic information can be stored within memory 294 and so that CHFtherapy can be properly controlled based upon the degree of severity.The CSR discrimination unit preferably operates only while the patientis asleep, as detected by a sleep detector 307. Additionally, inresponse to individual episodes of CSR, therapy controller 303 cancontrol implanted CSR alarm 14 or bedside alarm 18 to deliverappropriate warning or alarm signals to awaken the patient, in an effortto terminate the episode of CSR. If the patient is found to suffer fromchronic CSR-CSA or CSR-CHF, DAO pacing may be delivered in attempt toprevent the onset of additional episodes of CSR using DAO controller309. In addition, implantable drug pump 14 may be activated to delivermedications appropriate for the treatment of CSA or CHF. The operationof these components will be described in detail below with reference toFIG. 4. Finally, note that, although several of these internalcomponents are shown as being sub-components of the microcontroller,some or all may be implemented separately from the microcontroller.Depending upon the implementation, the various components of themicrocontroller may be separate software modules. The modules may becombined so as to permit a single module to perform multiple functions.

CSR Discrimination Unit and CHF Tracking Unit

Pertinent internal functional components of discrimination unit 301,therapy controller 303, and evaluation unit 305 are shown in FIG. 8.Discrimination unit 301 includes a CSR discrimination controller 350,which controls various components directed to the determination ofwhether episodes of CSR are caused by CSA or CHF. To this end, thecontroller activates a thoracic impedance detection unit 354, whichtracks variations in thoracic impedance caused by respiration based uponsignals received from one or more of the leads shown in FIG. 6. Asexplained more fully below, the impedance detection unit preferablyincludes internal filters for filtering out non-respiration-basedvariations in thoracic impedance, such as those caused by the beating ofthe heart. In any case, a CSR periodicity determination unit 356 isemployed to determine the time period or frequency associated with aparticular episode of CSR, using techniques also described in detailbelow. Once the periodicity has been determined, a discriminationthreshold comparison unit 358 compares the periodicity against a CSR-CSAvs. CSR-CHF discrimination threshold to identify the source or cause ofthe particular episode of CSR. The threshold itself is initiallydetermined by a threshold determination unit 360 based upon an analysisof previously-detected respiratory signals. Finally, a movementdetection unit 362 determines whether the patient is aroused from sleepor otherwise moves significantly during the discrimination process. Thisdetermination may employ physiologic sensor 308 of FIG. 7, which, asnoted, may be an accelerometer. In any case, if the patient is arousedduring episode of CSR or otherwise moves significantly in such a waythat the periodicity associated with CSR is significantly affected, thenthe discrimination process is deferred until the patient again fallsasleep or stops moving so that the periodicity can be reliablydetermined. An exemplary method used by the components of the CSRdiscrimination unit to discriminate CSR-CSA from CSR-CHF is describedbelow connection with FIGS. 9–11.

Turning now to therapy controller 303, the controller includes twocomponents: a CSA therapy controller 364 and a CHF therapy controller366. If CSR is caused by CSA, then the CSA therapy controller deliversappropriate therapy, in a manner described below primarily in connectionwith FIG. 12. If instead caused by CHF, then the CHF therapy controllerinstead of deliver appropriate CHF therapy, in a manner described belowprimarily in connection with FIG. 13.

CHF evaluation unit 305 includes an evaluation controller 368. Theevaluation controller activates a CHF severity lookup table comparisonunit 370 to compare the CSR periodicity value detected by unit 356 ofthe discrimination unit 301 with a set of look-up table values storedwithin memory 294. This is explained in greater detail below withreference to FIG. 14. A CHF progression tracking unit 372 tracks theprogression of CHF over an extended period of time based on long-termchanges in average CSR periodicity. This too is described below inconnection with FIG. 14.

Thus, FIG. 8 summarizes the internal functional components ofdiscrimination unit 301, therapy controller 303 and evaluation unit 305.Depending upon the implementation, the components may be configured asseparate software or hardware modules. The modules may be combined so asto permit single modules to perform multiple functions.

Exemplary CSR Discrimination Technique

One particular example of a CSR discrimination technique that may beperformed using the systems described above is set forth in FIGS. 9–13.Referring first to FIG. 9, at step 400, the pacer/ICD detects when thepatient falls asleep. Any of a variety of otherwise conventional sleepdetection techniques may be employed. Examples are set forth in thefollowing patents or patent applications: U.S. Pat. No. 5,476,483, toBornzin et al., entitled “System and Method for Modulating the Base RateDuring Sleep for a Rate-responsive Cardiac Pacemaker”; U.S. Pat. No.6,128,534 to Park et al., entitled “Implantable Cardiac StimulationDevice And Method For Varying Pacing Parameters To Mimic CircadianCycles”; and in U.S. patent application Ser. No. 10,339,989 of Koh etal., entitled “System And Method For Detecting Circadian States Using AnImplantable Medical Device”, filed Jan. 10, 2003.

Once the patient has fallen asleep then, at step 402, the pacer/ICDbegins track thoracic impedance (Z), at step 402. Thoracic impedance maybe detected using any of a variety of otherwise conventional techniques.An example is set forth the U.S. Pat. No. 5,817,135 to Cooper, et al.entitled, “Rate-Responsive Pacemaker with Noise-Rejecting Minute VolumeDetermination”. Preferably, the thoracic impedance values are filteredto eliminate variation in impedance caused by the beating of the heartor other non-respiratory factors. In one example, a low pass filter isemployed having a cutoff frequency set to some value greater than thefrequency of respiratory breathing but less than the frequencyassociated with the beating heart. For example, a cutoff frequency of 30cycles per minute may be employed. In addition, at step 402, thepacer/ICD updates a previously-determined discrimination threshold usinga technique described below in connection with FIG. 11. If adiscrimination threshold has not yet been calculated, a default value isinstead employed, such as a value in the range of 30 to 40 seconds.

At step 404, pacer/ICD detects the onset of an episode of CSR based uponbreathing patterns detected via thoracic impedance and any of a varietyof otherwise conventional CSR detection techniques can be employed,which exploit thoracic impedance. Alternatively, other techniques may beemployed such as techniques exploiting variations in A-V delay or R—Roscillations. Examples of CSR detection techniques are discussed in U.S.Pat. No. 6,600,949 to Turcott and in U.S. Patent to U.S. Pat. No.6,589,188 Street, et al., which are incorporated by reference herein.Assuming CSR has been detected then, at step 406, the pacer/ICD detectsperiods of sleep apnea occurring within CSR and determines theirduration. At step 408, bursts of breathing (i.e. hyperpnea) occurringduring CSR are detected and their durations are also measured.Preferably, the apnea durations and the hyperpnea durations are averagedover several cycles during CSR. While apnea and hyperpnea durations arebeing tracked, the pacer/ICD also monitors for arousal from sleep (orsignificant movement) using the accelerometer, at step 410, and, ifarousal is detected, the CSR discrimination process is aborted andprocessing instead returns to step 400 to again await detection ofanother sleep state. In this manner, potentially erroneous apnea andhyperpnea durations are discarded so that the values do not improperlyinfluence the determination of whether CSR is caused by CSA or CHF. Inany case, assuming that the patient is still asleep then, at step 412,the pacer/ICD determines the time period for the episode of CSR andbased upon the average durations of apnea and the average durations ofhyperpnea occurring following the periods of apnea.

FIG. 10 illustrates filtered impedance (denoted LP-Z) for an exemplaryepisode of CSR. As can be seen, changes in impedance reveal bursts ofhyperpnea 414 following each period of apnea 416. The duration of aperiod of apnea is identified by bracketed portion 418. The duration ofa period of hyperpnea is indicated by bracketed portion 420. The sum ofthe hyperpnea duration and the apnea duration collectively define thetime period for CSR. A burst of hyperpnea may be identified, forexample, by specifying an impedance variation threshold, above whichhyperpnea is presumed. If the variation in impedance remains below thatthreshold, apnea is presumed. This respiration detection thresholddiffers from the CSR discrimination threshold, discussed elsewhereherein. In any case, during an episode of CSR, time periods for at leasta few cycles of apnea/hyperpnea are tracked so as to provide an averagetime period value.

Returning to FIG. 9, at step 422, the CSR time period is comparedagainst the discrimination threshold updated at step 402 to identify thesource of the particular episode of CSR. If the time period is below thediscrimination threshold, then the episode of CSR is deemed to have beencaused by CSA (step 424) and CSR-CSA therapy is initiated, at step 426.Otherwise, if the time period exceeds the determination threshold thenCSR is deemed to have been caused by CHF (at step 428) and CSR-CHFtherapy is initiated at step 430. After steps 426 or 430, processingresumes at step 402 to detect the onset of any additional episodes ofCSR occurring while the patient is still asleep so that the cause of anysuch episodes can also be determined. As noted above, some patients aresubject to both CSR-CSA and CSR-CHF and so it is desirable to identifythe source of each episode of CSR.

Hence, FIG. 9 illustrates an exemplary method for discriminating CSR-CSAfrom CSR-CHF based upon CSR time periods as determined based upon aseparate calculation of apnea time periods and hyperpnea time periods.Alternative techniques may instead be employed for detecting the timeperiod. For example, the duration from one hyperpnea burst to anothermay instead be employed by, for example, detecting the peak or midpointof consecutive breathing bursts. However, separate detection of thedurations of the apnea time periods and the hyperpnea time periods isbelieved to be more reliable and hence is preferred. In addition,frequency values for CSR can instead be exploited.

Referring now to FIG. 11, an exemplary technique for determining andupdating the discrimination threshold will now be described for useduring step 402 of FIG. 9. Initially, at step 432, a low pass filter isapplied to the thoracic impedance signals (if the impedance signals havenot already in filtered) to eliminate variations caused by the beatingof the heart or other non-respiratory factors. The resulting filteredimpedance signal is illustrated in FIG. 10 and has already beendiscussed. Then, at step 434, the filtered impedance signal isdifferentiated, i.e. the mathematical derivative of the filtered signalis calculated, herein denoted dZ. With the filtered impedance signalrepresented internally by digital values, standard digital techniquesare employed to calculate (dZ). The differentiated signal dZ is shown inFIG. 10 as graph 436. Next, at step 436, zero crossing points areidentified within the differentiated signal dZ. The zero crossing pointscorrespond to peaks and valleys within the original filtered impedancesignal.

At step 438, the differentiated signal dZ is then integrated betweenconsecutive zero crossing points to generate a set of amplitude values,indicative of valley-to-peak amplitude variations. With dZ representedinternally by digital values, standard digital techniques are employedto integrate or sum dZ to generate the individual amplitude values.Individual integrated values are shown within FIG. 10 as graph 440. Eachindividual value within graph 414 thereby provides a measure of thevariation from a negative valley to a next positive peak within thefiltered impedance signal. Hence, these values are indicative of therange of physical movement of the thorax from maximum contraction tomaximum expansion during a respiration cycle. During apnea, of course,there is little or no variation since the patient is not breathing.During periods of hyperpnea, significant variation occurs. Hence, theintegrated values provide a clear indication of periods of hyperpnea andperiods of apnea. At step 442, a moving average of the integrated valuesis calculated. It is this moving average that is used as the CHFdiscrimination threshold of FIG. 9. The moving average is shown withinFIG. 10 as line 444. If the average time period associated with a givenepisode of CSR clearly exceeds the threshold, CSR-CHF is deemed to beoccurring. If the average time period associated with a given episode ofCSR is clearly below the threshold, CSR-CSA is deemed to be occurring.If the average value is near the threshold, it is rejected and CSRdiscrimination is deferred until more average time period values aredetected that are clearly above or below the threshold.

Hence, FIGS. 9–11 illustrate one possible technique for calculating athreshold for use in discriminating CSR-CHF from CSR-CSA based upon theperiodicity of CSR. Other techniques may alternatively be employed. Notethat, since the integrated values of graph 444 of FIG. 10 provide aclear indication of periods of hyperpnea and periods of apnea, theintegrated values can additionally be used for calculating the timeperiods associated with CSR during steps 406–412. For example, periodsof hyperpnea may be calculated by determining whether the integratedvalues exceed a hyperpnea threshold. Likewise, a period of apnea may bedetected by determining when the integrated values fall below thehyperpnea threshold.

CSR-CSA and CSR-CHF Therapy

CSR-CSA therapy is summarized in FIG. 12. Two forms of therapy areprovided: long-term therapy and short-term therapy. Long-term therapy ispreferably employed at all times within patients who are found to besubject to frequent episodes of CSR-CSA. Short-term therapy is appliedonly during individual episodes of CSR-CSA. Long-term therapy, performedat step 452, includes DAO pacing therapy applied in an attempt toprevent the onset of additional episodes of CSR-CSA. A particularlyeffective overdrive pacing technique for the atria, referred to hereinas dynamic atrial overdrive (DAO) pacing, is described in U.S. Pat. No.6,519,493 to Florio et al., entitled “Methods And Apparatus ForOverdrive Pacing Heart Tissue Using An Implantable Cardiac StimulationDevice”. With DAO, the overdrive pacing rate is controlled to remaingenerally uniform and, in the absence of a tachycardia, is adjustedupwardly or downwardly only occasionally. The aggressiveness ofoverdrive pacing may be modulated by adjusting the overdrive pacing rateand related control parameters. See: U.S. patent application Ser. Nos.10/093,225 and 10/092,695, both of Florio et al., entitled “Method AndApparatus For Using A Rest Mode Indicator To Automatically AdjustControl Parameters Of An Implantable Cardiac Stimulation Device”, bothfiled Mar. 6, 2002; U.S. patent application Ser. No. 10/043,781, also ofFlorio et al., entitled “Method And Apparatus For Dynamically AdjustingA Non-Linear Overdrive Pacing Response Function”, filed Jan. 9, 2002;and U.S. patent application Ser. No. 10/043,472, of Florio et al.,entitled “Method And Apparatus For Dynamically Adjusting OverdrivePacing Parameters”, filed Jan. 9, 2002. These DAO applications areincorporated by reference herein. Preferably, parameters for controllingDAO therapy are set to values appropriate for reducing the likelihood ofadditional episodes of CSR-CSA. Routine instrumentation may be performedto identify optimal DAO pacing parameters for use with patients withCSR-CSA. The aggressiveness of DAO therapy may be adjusted based uponthe frequency or duration of episodes of CSA occurring during CSR-CSA.

Long-term CSR-CSA therapy also includes the delivery of anti-apneamedications via an implantable drug pump, if so equipped. Examples ofmedications that may be helpful in patients with apnea are set forth thefollowing patents: U.S. Pat. No. 6,331,536 to Radulovacki, et al.,entitled “Pharmacological Treatment for Sleep Apnea”; U.S. Pat. No.6,432,956 to Dement, et al. entitled “Method for Treatment of SleepApneas”; U.S. Pat. No. 6,586,478 to Ackman, et al., entitled “Methodsand Compositions for Improving Sleep”; and U.S. Pat. No. 6,525,073 toMendel, et al., entitled “Prevention or Treatment of Insomnia with aNeurokinin-1 Receptor Antagonist”. Depending upon the particularmedication, alternative compounds may be required for use in connectionwith an implantable drug pump. Routine experimentation may be employedto identify medications for treatment of sleep apnea that are safe andeffective for use in connection with an implantable drug pump. Dosagesmay be titrated based upon the frequency or duration of episodes of CSAoccurring during CSR-CSA.

Short-term CSR-CSA therapy, performed at step 450, involves triggeringan implantable CSR alarm (such as alarm 14 of FIG. 1) to awaken thepatient in an attempt to terminate the episode of CSR-CSA.Alternatively, a bedside alarm may be activated by transmission ofappropriate wireless control signals. As already noted, activation of analarm to awaken the patient is preferably employed only if long-termtherapy is found to be ineffective, since awakening the patientinterrupts with the patient's natural sleeping patterns. In any case,whenever some form of CSA therapy is delivered, appropriate diagnosticinformation is stored at step 454 so that if medical professional cansubsequently review the therapy and evaluate its effectiveness.

If implantable phrenic nerve stimulators are implanted, short-termtherapy can also involve delivery of rhythmic electrical stimulation tothe phrenic nerves to mimic breathing. Examples of phrenic nervestimulators are set forth in U.S. Pat. No. 5,056,519 to Vince, entitled“Unilateral Diaphragmatic Pacer” and in U.S. Pat. No. 6,415,183 toScheiner, et al., entitled “Method and Apparatus for DiaphragmaticPacing”, which are incorporated by reference herein. Other respiratorynerves may be stimulated as well. U.S. Pat. No. 5,911,218 to DiMarco,entitled “Method and Apparatus for Electrical Stimulation of theRespiratory Muscles to Achieve Artificial Ventilation in a Patient”describes stimulation of nerves leading to intercostal muscles.

CSR-CHF therapy is summarized in FIG. 13. Again, two forms of therapyare provided: long-term therapy and short-term therapy. Long-termtherapy is preferably employed at all times within patients found to besubject to frequent periods of CSR-CHF whereas short-term therapy isapplied only during individual episodes of CSR-CHF. Long-term therapy,performed at step 460, may include use of CRT to improve cardiacfunction. CRT is primarily applied to counteract the debilitatingeffects CHF but can also be helpful in preventing additional episodes ofCSR-CHF. CRT may be performed in accordance with otherwise conventionaltechniques, such as those set forth in the aforementioned patents toMathis, et al., Kramer, et al. and Stahmann, et al. Additionally, or inthe alternative, DAO pacing therapy is applied in an attempt to preventthe onset of additional episodes of CSR-CHF. Again, preferably, theparameters for controlling DAO therapy are set to values appropriate forreducing the likelihood of additional episodes of CSR-CHF and routineexperimentation may be performed to identify such optimal parameters.Note that the specific parameters for controlling DAO therapy to preventthe onset of CSR-CHF may differ from the parameters for controlling DAOto prevent the onset of CSR-CHF. Hence, if a particular patient is onlysubject to CSR-CHF but not CSR-CSA, a different set of controlparameters may be employed than if the patient is subject to both.Long-term CSR-CHF therapy also includes delivery of CHF medications viaan implantable drug pump, if so equipped. Exemplary CHF medicationsinclude ACE inhibitors, diuretics, digitalis and compounds such ascaptopril, enalapril, lisinopril and quinapril. Depending upon theparticular medication, alternative compounds may be required for use inconnection with an implantable drug pump. Routine experimentation may beemployed to identify medications for treatment of CHF that are safe andeffective for use in connection with an implantable drug pump. Dosagesmay be titrated based upon the frequency or duration of episodes of CSRoccurring as a result of CHF.

Short-term CSR-CHF therapy, performed at step 462, includes use of theimplantable CSR alarm or external bedside alarm to awaken the patient.Again, activation of an alarm to awaken the patient is preferablyemployed only if other forms of therapy are found to be ineffective. Inany case, whenever some form of CSR-CHF therapy is delivered,appropriate diagnostic information is stored at step 464.

Exemplary CSR Severity Evaluation Technique

One particular example of a CHF severity evaluation technique that maybe performed using the systems described above is set forth in the FIG.14. In this example, the severity of CHF is evaluated based on CSRoccurring while patient is asleep and any arousal from sleep during theevaluation process is also detected. In other examples, the severity ofCHF may be evaluated based on CSR occurring while the patient is awake.The steps of detecting sleep and monitoring for arousal from sleep areprovided for the sake of completeness. In addition, several of the stepsare similar to those of the technique of FIG. 9 and, accordingly, suchsteps are not described again in detail.

At step 500 of FIG. 14, the pacer/ICD detects when the patient fallsasleep and then, at step 502, tracks thoracic impedance Z, at step 502.Note that the pacer/ICD need not calculate a discrimination threshold asin FIG. 9. At step 504, the pacer/ICD detects the onset of an episode ofCSR using otherwise conventional techniques. Assuming CSR has beendetected then, at step 506, the pacer/ICD detects periods of sleep apneaoccurring within CSR and then determines their duration and, at step508, detects bursts of hyperpnea and determines their durations as well.Again, preferably, the apnea durations and the hyperpnea durations areaveraged over several cycles during CSR. While apnea and hyperpneadurations are being tracked, the pacer/ICD also monitors for arousalfrom sleep using the accelerometer, at step 510, and if arousal isdetected the CHF severity evaluation process is aborted and processinginstead returns to step 500 to again await detection of another sleepstate. Assuming that the patient is still asleep then, at step 512, thepacer/ICD determines the time period for the episode of CSR based uponthe average durations of apnea and the average durations of hyperpnea.At step 514, the time period is compared against a range of valuesrepresentative of different degrees of severity of CHF derived for thepatient. Preferably, the range of values is set based upon a baselinevalue of CSR periodicity obtained for the particular patient. Forexample, if a physician examines the patient and determines that CSR isstill mild, the current CSR time period for the patient may then be usedas a baseline for specifying ranges values corresponding to mild CSR andcorresponding to more severe forms of CSR for the patient.

Exemplary values for a hypothetical patient are set forth in TABLE I. Inthis example, the baseline periodicity for mild CSR within the patientis in the range of 40 to 50 seconds. From that baseline periodicity,ranges of values corresponding to more severe CSR are specified, so thatchanges in the severity of CSR may be tracked within the patient. Theranges of values may be specified by the physician or may be generatedby the pacer/ICD based upon data input by the physician. For a differentpatient, a different baseline periodicity may be obtained and differentvalues for the various levels of severity may be specified. The valuesof TABLE I are hypothetical values provided merely for illustrating theinvention. Although only four classifications are showing TABLE I, theseverity of CHF may be further subdivided into more additionalclassification levels. If CSR periodicity is instead calculated based onfrequency, then corresponding frequency ranges are instead employed.

TABLE I CSR TIME PERIOD (in seconds) SEVERITY CLASSIFICATION 40–50 Mild51–65 Moderate 61–80 Severe above 80 Very Severe

At step 516, CHF therapy is controlled based upon the degree ofseverity. CHF therapy is discussed above in connection with FIG. 13. Thedegree of severity may be used, for example, to control CRT pacingparameters, such as the time delay between left and right ventricularpulses or to control pharmacological CHF therapy to, for example, selectthe type of pharmacological agents to be delivered via the implantabledrug pump or to titrate dosages. At step 518, the pacer/ICD tracks theprogression of CHF based on long-term changes in CHF severity, such aschanges occurring over weeks or months. To this end, the pacer/ICDstores individual values indicative of CHF severity, such as the CSRtime period value, and then periodically compares newly-detected CSRtime period values against previous ones to track CHF progression.Appropriate diagnostic information is stored so that a physician canreview the data during a follow-up session. If a significant progressionin CHF occurs and if the system is so equipped, warning signals can betransmitted to the bedside monitor for immediate relay to the physician,perhaps via telephonic transmission, so that the physician is therebypromptly advised of the change in status.

Hence, FIG. 14 illustrates one possible technique for evaluating theseverity of CHF. Others techniques may be performed in accordance withthe general principles of the invention.

What have been described are various systems and methods for detectingCSR, distinguishing between CSR-CSA and CSR-CHF, evaluating the severityof CHF based on CSR, and delivering and controlling therapy in responsethereto using an implantable system controlled by a pacer or ICD.However, principles of the invention may be exploiting using otherimplantable systems or in accordance with other techniques. Thus, whilethe invention has been described with reference to particular exemplaryembodiments, modifications can be made thereto without departing fromthe spirit and scope of the invention.

1. A system for evaluating the severity of congestive heart failure(CHF) within a patient using an implanted medical device wherein thepatient also exhibits Cheyne-Stokes Respiration (CSR) caused by CHF, thesystem comprising: a CSR periodicity determination unit operative todetermine a periodicity associated with CSR for the patient; a CSRperiodicity-based CHF evaluation unit operative to evaluate the severityof CHF within the patient based on the periodicity; and a CHF therapycontroller operative to control delivery of therapy to the patient basedon the evaluation of the severity of CHF.
 2. A system for evaluating theseverity of congestive heart failure (CHF) within a patient using animplanted medical device wherein the patient also exhibits Cheyne-StokesRespiration (CSR) caused by CHF, the system comprising: a CSRperiodicity determination unit operative to determine a periodicityassociated with CSR for the patient; a CSR periodicity-based CHFevaluation unit operative to evaluate the severity of CHF within thepatient based on the periodicity; an implantable drug pump; and controlcircuitry connected to the CSR periodicity-based CHF evaluation unit andto the implantable drug pump and operative to control at least one ofthe dosage and the type of drug delivered via the drug pump based on theseverity of CHF.
 3. A method for evaluating the severity of congestiveheart failure (CHF) within a patient using an implanted medical devicewherein the patient also exhibits Cheyne-Stokes Respiration (CSR) causedby CHF, the method comprising: detecting a time period representative ofperiodic breathing during CSR in the patient by: detecting an episode ofCSR; and determining the average duration of periods of apnea during theepisode of CSR, determining the average duration of periods of breathingbetween the periods of apnea during CSR, and combining the averageduration of periods of apnea with the average duration of periods ofbreathing; and evaluating the severity of CHF within the patient basedon the periodicity.
 4. The method of claim 3 wherein determining theaverage duration of periods of sleep apnea during CSR and determiningthe average duration of periods of breathing between the periods ofsleep apnea during CSR are performed using one or more of thoracicimpedance, AV delay, and R—R oscillations.
 5. A method for evaluatingthe severity of congestive heart failure (CHF) within a patient using animplanted medical device wherein the patient also exhibits Cheyne-StokesRespiration (CSR) caused by CHF, the method comprising: detecting aperiodicity associated with CSR in the patient; and evaluating theseverity of CHF within the patient by comparing the periodicityassociated with CSR against a set of values indicative of the severityof CHF.
 6. The method of claim 5 further comprising storing a valueindicative of the current severity of CHF in a memory.
 7. A system forevaluating the severity of congestive heart failure (CHF) within apatient using an implanted medical device wherein the patient alsoexhibits Cheyne-Stokes Respiration (CSR) caused by CHF, the systemcomprising: a CSR periodicity determination unit operative to determinea periodicity associated with CSR for the patient; a CSRperiodicity-based CHF evaluation unit operative to evaluate the severityof CHF within the patient based on the periodicity; a pacing pulsegenerator operative to generate overdrive pacing pulses for delivery tothe heart of the patient; and control circuitry connected to the CSRperiodicity-based CHF evaluation unit and to the pacing pulse generatorand operative to control the aggressiveness of overdrive therapy basedon the severity of CHF.
 8. A method for evaluating the severity ofcongestive heart failure (CHF) within a patient using an implantedmedical device wherein the patient also exhibits Cheyne-StokesRespiration (CSR) caused by CHF, the method comprising: detecting aperiodicity associated with CSR in the patient; evaluating the severityof CHF within the patient based on the periodicity; and deliveringtherapy to the patient based on the severity of CHF; wherein animplantable drug pump is provided and wherein delivering therapycomprises delivering CHF drug therapy to the patient using the drug pumpand wherein the dosage or the type of drug is selected based on thedegree of severity of CHF.
 9. A method for evaluating the severity ofcongestive heart failure (CHF) within a patient using an implantedmedical device wherein the Patient also exhibits Cheyne-StokesRespiration (CSR) caused by CHF, the method comprising: detecting aperiodicity associated with CSR in the patient; evaluating the severityof CHF within the patient based on the periodicity; and deliveringlong-term therapy in response to the detection of frequent episodes ofCRS caused by CHF (CSR-CHF) by delivering overdrive pacing therapy tothe heart of the patient with the aggressiveness of overdrive therapyadjusted based on the degree of severity of CHF.
 10. A method forevaluating the severity of congestive heart failure (CHF) within apatient using an implanted medical device wherein the patient alsoexhibits Cheyne-Stokes Respiration (CSR) caused by CHF, the methodcomprising; detecting a periodicity associated with CSR in the patient;evaluating the severity of CHF within the patient based on theperiodicity; and verifying that the CSR of the patient is caused by CHFand not central sleep apnea (CSA) based on the periodicity.
 11. A methodfor determining the severity of congestive heart failure (CHF) within apatient using an implanted medical device wherein the patient alsoexhibits Cheyne-Stokes Respiration (CSR) caused by CHF, the methodcomprising: tracking a periodicity associated with CSR for the patient;detecting changes over time in the periodicity associated with CSR; anddetecting one of progression or regression of CHF within the patientover time based on the changes in the periodicity, wherein an increasein a time period of CSR corresponds to progression of CHF.
 12. A systemfor evaluating the severity of congestive heart failure (CHF) within apatient using an implanted medical device wherein the patient alsoexhibits Cheyne-Stokes Respiration (CSR) caused by CHF, the systemcomprising: a CSR periodicity determination unit operative to determinea periodicity associated with CSR for the patient; a CSRperiodicity-based CHF evaluation unit-operative to evaluate the severityof CHF within the patient by comparing the periodicity associated withCSR against a set of values indicative of the severity of CHF.